We have found that a G-protein coupled receptor FPR is selectively expressed by highly malignant human glioblastoma cells. Activation of FPR promotes tumor cell chemotaxis, survival and production of angiogenic facotr VEGF. Knocking down FPR by small interfering RNA markedly reduces the capacity of glioblastoma cells to form tumors in nude mice. In addition, FPR is activated by agonist activity contained in the supernatants of necrotic tumor cells. Thus, FPR acts as a sensor on glioblastoma cells for agonists produced in the tumor environment to exacerbate the progression of the tumor.